Demyelination is the major underlying factor
responsible for the symptoms of multiple sclerosis (MS). Demyelination
is the destructive removal of myelin, an insulating
and protective fatty protein which sheaths nerve cells (neurons).
More specifically, the myelin is wrapped around the long extensions of
neurons called axons. During MS relapses,
patches of white matter in the central
nervous system that normally contain tracts of myelinated neurons become
inflamed and lose their myelin. These patches of demyelination are known
as lesions.

The cause and precise mechanism of demyelination is not
clearly understood but there is good evidence that the body's own immune
system is at least partially responsible. Acquired
immune system cells called T-cells are known
to be present at the site of lesions. Other immune system cells called
macrophages (and possibly mast
cells as well) also contribute to the damage.

Myelin is produced by special "glial cells"
in the central nervous system called oligodendrocytes.
Oligodendrocytes and axons have a many to many relationship - that is one
oligodendrocyte produces myelin for several axons and one axon has several
oligodendrocytes producing its myelin. In MS, it is not just the myelin
that is destroyed but also these oligodendrocytes and occasionally even
the axons themselves.

Axons use an electrochemical mechanism to transmit nerve
impulses - the action potential. This
requires sodium and potassiumions to pass
through a semi-permeable membrane around the nerve. It is believed that
the myelin not only insulates and encases this electrochemical process
but also actively assists it. When axons become demyelinated, they transmit
the nerve impulses 10 times slower than normal myelinated ones.

During periods of MS remission,
the oligodendrocytes repair the damaged axons in a process called remyelination.
However, very often the oligodendrocytes are also destroyed which delays
or prevents remyelination from happening. Additionally, another kind of
glial cell, called astrocytes, cause scar
tissue to form in place of the myelin. Scar tissue does not perform the
same function as the myelin. As the disease reaches its more advanced phases,
the axons themselves are often destroyed as well.